Hormonal changes in cerebral infarction in the young and elderly

Elwan, Osamah; Abdallah, Mohamed; Issa, Ibrahim; Taher, Y; El-Tamawy, Mohamed S.

doi:10.1016/0022-510x(90)90264-n

Cited by 14 publications

(11 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Lowered testosterone levels have been found in Alzheimer's disease [41], stroke [42], and Parkinson's disease [43].…”

Section: Changes In the Regulation Of Testosterone Synthesismentioning

confidence: 99%

The Paradox Dividing Testosterone Deficiency Symptoms and Androgen Assays: A Closer Look at the Cellular and Molecular Mechanisms of Androgen Action

Carruthers

2008

The Journal of Sexual Medicine

View full text Add to dashboard Cite

Introduction Central to the diagnosis and treatment of testosterone deficiency syndrome in the adult male is the remarkable paradox that there is a very poor correlation between the characteristic symptoms and levels of serum androgens. Aim Because androgen deficiency can be associated with severe symptomatology, as well as diverse conditions such as coronary heart disease, diabetes, and metabolic syndrome, the aim was to present an evidence-based working hypothesis to resolve this confusing clinical paradox. Methods A review of the possible mechanisms in testosterone deficiency syndrome was carried out, and a hypothesis to explain this paradox and associated problems in the diagnosis and clinical management of androgen deficiency was established on the basis of a review of the literature. Main Outcome Measures The mechanisms by which androgen deficiency could arise were studied at five different levels: Results As with insulin in maturity onset diabetes mellitus, there can be both insufficient production and variable degrees of resistance to the action of androgens operating at several levels in the body simultaneously, with these factors becoming progressively worse with aging, adverse lifestyle, other disease processes, and a wide range of medications. Conclusions Using this model, androgen deficiency can be redefined as an absolute or relative deficiency of androgens or their metabolites according to the needs of that individual at that time in his life. There are important ways in which the considerations raised by this hypothesis affect the etiology, terminology, diagnosis, and treatment of androgen-deficient states.

show abstract

“…Lowered testosterone levels have been found in Alzheimer's disease [41], stroke [42], and Parkinson's disease [43].…”

Section: Changes In the Regulation Of Testosterone Synthesismentioning

confidence: 99%

The Paradox Dividing Testosterone Deficiency Symptoms and Androgen Assays: A Closer Look at the Cellular and Molecular Mechanisms of Androgen Action

Carruthers

2008

The Journal of Sexual Medicine

View full text Add to dashboard Cite

show abstract

“…A brief review of this adult literature illustrates that studies using an induced injury model simulating adult stroke—middle cerebral artery occlusion (MCAO)—show consistent evidence that males benefit after injury from acute testosterone depletion, while the presence of testosterone increases glutamate toxicity following injury [37]. Furthermore, testosterone and its metabolite dihydrotestosterone (DHT) have been shown to increase stroke damage in young adult rats [37, 66, 67], while testosterone concentration was found to be inversely associated with stroke severity and 6-month mortality [68, 69]. Interestingly, young male rats were also found to incur larger strokes than their older counterparts, an effect hypothesized to be due to the ability of testosterone to alter the susceptibility of the brain to ischemic damage in an age-dependent manner.…”

Section: Early Hormonal Factorsmentioning

confidence: 99%

“…It should be noted that the effects of estrogen on adult human stroke are less clear, and many of the successful studies of estrogen replacement in animal models have failed to translate to human clinical populations [75, 76]. Nonetheless, whatever the protective mechanism(s) of estrogen may be, they are less likely to fully account for the neonatal effects described here, since female protection has been shown in animal models of neonatal brain injury, when minimal circulating estrogen from the quiescent neonatal ovaries is present [40, 68, 72, 73, 81, 82] although central steroidogenesis may occur [64]. Still, it is certainly possible that some late developmental beneficial effects of ovarian estrogen on neural reorganization after injury could occur.…”

Section: Early Hormonal Factorsmentioning

confidence: 99%

Sex Differences in Mechanisms and Outcome of Neonatal Hypoxia-Ischemia in Rodent Models: Implications for Sex-Specific Neuroprotection in Clinical Neonatal Practice

Hill

Fitch

2012

Neurology Research International

169

144

View full text Add to dashboard Cite

Clinical findings show that male infants with hypoxic-ischemic injury (HI) fare more poorly than matched females on cognitive outcomes. Rodent models of neonatal hypoxia-ischemia support this difference, with data showing that perinatal brain injury leads to long-term behavioral deficits primarily in male rodents and in female rodents treated with early androgens. Results support the idea that sex-specific gonadal hormones may modulate developmental response to injury and dovetail with overwhelming evidence of developmental androgen effects on typical brain morphology and behavior. However, mechanisms underlying sex differences in response to early brain injury may be more complicated. Specifically, activation of cell death pathways in response to HI may also differ by sex. In females, the preferential activation of the caspase-dependent apoptotic pathway may actually afford greater protection, potentially due to the actions of X-linked inhibitor of apoptosis (XIAP) within this pathway. This contrasts the pattern of preferential activation of the caspase-independent pathway in males. While an integrated model of sex-specific hormonal and genetic modulation of response to early injury remains to be fully elucidated, these findings suggest that infants might benefit from sex-specific neuroprotection following HI injury.

show abstract

“…Testosterone levels are reduced after a variety of kinds of stress (Norman and Smith, 1992;Tohei et al, 1997;Friedl et al, 2000;Morgan et al, 2000). Testosterone levels decrease after stroke, and concentrations of testosterone are inversely associated with stroke severity and 6 month mortality (Elwan et al, 1990;Jeppesen et al, 1996). Anesthesia can also decrease testosterone level (Sanhouri et al, 1990).…”

Section: Introductionmentioning

confidence: 98%

Neuroendocrine mechanism for tolerance to cerebral ischemia-reperfusion injury in male rats

et al. 2005

View full text Add to dashboard Cite

Testosterone has been shown to exacerbate cerebral ischemia-reperfusion injury, which suggests that the well-known stress-induced testosterone reduction could be a protective response. We hypothesized that stress-induced testosterone reduction contributes to ischemia tolerance in cerebral ischemia-reperfusion injury in male rats. In intact male rats, stress was induced by brief anesthesia at 6 h before transient middle cerebral artery occlusion (MCAO). Testosterone levels were significantly decreased 6 h after stress. Testosterone reduction was associated with a 50% reduction in cerebral lesion volume in the stressed animals. Further, the stress-induced cerebral ischemia tolerance was eliminated by testosterone replacement in castrated males. Immunohistochemical staining showed that androgen receptors were up-regulated after cerebral ischemia-reperfusion injury and partially colocalized with terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) positive cells in the parietal cortex and extensively colocalized in the caudate putamen. Heat shock protein 70 (Hsp70) and 90 (Hsp90) are involved in ischemia tolerance, and were not colocalized with TUNEL in the immunohistochemical staining, suggesting an antiapoptotic role of Hsp's. To determine the effect of testosterone on MCAO-induced Hsp70 and -90 expression, a testosterone replacement or withdrawal paradigm was used. Testosterone-replaced animals exhibited a decrease in Hsp expression, whereas testosterone withdrawal (mimicking the stress-induced testosterone suppression) normalized this deficit. In summary, stress-induced testosterone reduction contributes to ischemia tolerance in cerebral ischemia-reperfusion injury in males, which could be related to the loss of inhibition by testosterone of Hsp70 and -90 expression.

show abstract

Hormonal changes in cerebral infarction in the young and elderly

Cited by 14 publications

References 29 publications

The Paradox Dividing Testosterone Deficiency Symptoms and Androgen Assays: A Closer Look at the Cellular and Molecular Mechanisms of Androgen Action

The Paradox Dividing Testosterone Deficiency Symptoms and Androgen Assays: A Closer Look at the Cellular and Molecular Mechanisms of Androgen Action

Sex Differences in Mechanisms and Outcome of Neonatal Hypoxia-Ischemia in Rodent Models: Implications for Sex-Specific Neuroprotection in Clinical Neonatal Practice

Neuroendocrine mechanism for tolerance to cerebral ischemia-reperfusion injury in male rats

Contact Info

Product

Resources

About